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Cardiovascular System & Hypertension — Comprehensive Study Notes Flashcards

Master Cardiovascular System & Hypertension — Comprehensive Study Notes with these flashcards. Review key terms, definitions, and concepts using active recall to strengthen your understanding and ace your exams.

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Cardiovascular System

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The organ system made up of the heart, blood, and blood vessels that transports substances throughout the body. It delivers oxygen and nutrients to tissues and removes waste products. It also works with the lungs to oxygenate blood and remove CO2CO_2.

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Cardiovascular System

Back

The organ system made up of the heart, blood, and blood vessels that transports substances throughout the body. It delivers oxygen and nutrients to tissues and removes waste products. It also works with the lungs to oxygenate blood and remove $CO_2$.

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Blood Vessels

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Hollow tubular structures that transport blood throughout the body and come in three major types: arteries, veins, and capillaries. Each type differs in structure and function to accommodate pressure and exchange needs. They form the circulation routes for systemic and pulmonary circuits.

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Arteries

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Vessels that carry blood away from the heart and typically endure higher pressure than veins. They have thicker walls, especially a prominent tunica media, to withstand and regulate pressure. Examples include the aorta and muscular arteries supplying organs.

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Veins

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Vessels that return blood toward the heart and generally operate under lower pressure than arteries. They have thinner walls and larger lumens and can accommodate large blood volumes. Many veins contain valves to help ensure one-way flow back to the heart.

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Capillaries

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The smallest blood vessels that directly connect arterioles and venules and provide exchange of oxygen, $CO_2$, nutrients, and waste with tissue cells. They form dense networks called capillary beds to maximize contact with tissues. Their thin walls facilitate diffusion.

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Overall Blood Flow

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Starts with the left ventricle pumping oxygenated blood into the aorta, which moves through arteries, arterioles, and capillaries where oxygen diffuses to tissues. Deoxygenated blood then returns via venules and veins to the right ventricle and pulmonary circulation. The cycle repeats continuously.

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Superior Vena Cava

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A great vessel that returns oxygen-poor blood from regions above the diaphragm to the right atrium. It is one of the primary systemic venous return pathways. It delivers deoxygenated blood from head, neck, and upper limbs.

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Inferior Vena Cava

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A great vessel that returns oxygen-poor blood from regions below the diaphragm to the right atrium. It collects blood from the abdomen, pelvis, and lower limbs. It is the largest vein in the body by diameter.

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Pulmonary Trunk

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The vessel that carries oxygen-poor blood from the right ventricle to the lungs for gas exchange and branches into the right and left pulmonary arteries. It is the beginning of the pulmonary circulation. It directs deoxygenated blood to the pulmonary capillaries.

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Pulmonary Veins

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A set of four veins (right and left, superior and inferior) that return oxygen-rich blood from the lungs to the left atrium. They are unique as veins that carry oxygenated blood. They complete pulmonary circulation by delivering oxygenated blood to the heart.

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Aorta

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The largest artery in the body that carries oxygen-rich blood from the left ventricle to the systemic circulation. It is an elastic artery that helps maintain blood flow during diastole. It branches into arteries supplying all major organ systems.

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Heart Size

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Roughly the size of a fist and weighs less than one pound in the average adult. It is protected anteriorly by the sternum and posteriorly by the spinal column, flanked by lungs, and rests on the diaphragm. Positioning aids protection and functional orientation.

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Pulmonary Circuit

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The right-side pathway of the heart that receives deoxygenated blood from the body and pumps it to the lungs to release $CO_2$ and pick up oxygen. It involves the right atrium, right ventricle, pulmonary trunk, pulmonary arteries, lungs, and pulmonary veins. Its primary role is gas exchange.

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Systemic Circuit

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The left-side pathway that receives oxygenated blood from the lungs and pumps it to body tissues via the aorta and systemic arteries. It supplies oxygen and nutrients to organs and removes metabolic wastes. It maintains tissue perfusion and organ function.

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Pericardium

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A membranous sac that surrounds and protects the heart, providing a lubricated environment for movement. It consists of fibrous and serous layers that stabilize the heart within the thorax. It reduces friction between the heart and surrounding structures.

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Epicardium

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The outermost layer of the heart wall lying just beneath the pericardium that gives the heart a smooth, slippery surface. It contains blood vessels and nerves supplying the myocardium. It also contributes to the serous layer of the pericardium.

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Myocardium

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The thick middle layer of the heart wall composed of cardiac muscle responsible for contraction and pumping action. Thickness varies by chamber, being greatest in the left ventricle. It generates the force needed to circulate blood throughout the body.

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Endocardium

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The innermost layer of the heart composed of endothelium that lines the four chambers and valves, providing a smooth surface to reduce friction as blood flows. It helps maintain a non-thrombogenic interior. It also contributes to valvular structure.

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Atria

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The two superior heart chambers (right and left atria) that receive venous blood and channel it into the ventricles. Right atrium collects deoxygenated systemic blood; left atrium receives oxygenated pulmonary blood. They act primarily as receiving reservoirs and aid ventricular filling.

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Ventricles

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The two inferior chambers (right and left ventricles) that pump blood out of the heart to the pulmonary and systemic circulations. The right ventricle pumps to the pulmonary trunk and lungs; the left ventricle pumps to the aorta and systemic tissues. Ventricular contraction generates systemic and pulmonary pressures.

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AV Valves

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Atrioventricular valves located between each atrium and its ventricle that allow blood to flow from higher-pressure atrium into a lower-pressure ventricle. The tricuspid valve is on the right and the mitral (bicuspid) valve is on the left. They prevent backflow during ventricular contraction.

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Semilunar Valves

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Valves that permit blood to flow out of the ventricles into the pulmonary artery and aorta and prevent backflow into the ventricles during diastole. They are the pulmonary and aortic valves. Each has three cusps shaped like half-moons.

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STEMI

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A type of myocardial infarction characterized by a complete obstruction of coronary blood flow, typically producing ST-elevation on ECG. It usually indicates transmural ischemia and requires urgent reperfusion. It carries higher immediate mortality risk than partial occlusions.

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NSTEMI

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A myocardial infarction caused by partial obstruction of coronary blood flow that typically does not show ST-elevation on ECG but still indicates myocardial injury. Management focuses on stabilization and assessment for revascularization as needed. It may be less immediately catastrophic than STEMI but still serious.

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Tunica Intima

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The innermost vascular tunic composed of endothelium that provides a slick surface to reduce friction as blood flows through the lumen. It plays a key role in vascular homeostasis and barrier function. Endothelial injury here is central to atherosclerosis development.

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Tunica Media

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The middle vascular tunic composed mainly of smooth muscle and elastic fibers that regulates vessel diameter under nervous and chemical control. It mediates vasodilation and vasoconstriction, influencing blood pressure and distribution. Its thickness is greater in arteries than veins.

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Tunica Externa

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The outermost vascular tunic made of loose collagen fibers that protect, reinforce, and anchor vessels to surrounding tissues. It contains nerves and, in larger vessels, small blood vessels (vasa vasorum). It provides structural support and flexibility.

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Elastic Arteries

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Large arteries near the heart (such as the aorta) with thick elastic walls that smooth out pressure fluctuations from ventricular contraction and maintain continuous blood flow. They tolerate high systolic pressure and help maintain diastolic pressure through recoil. They are the largest-diameter arteries.

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Muscular Arteries

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Medium-sized arteries that distribute blood to specific organs and have a relatively thick tunica media for vasomotor control. They regulate regional blood flow by contracting or dilating. They lie downstream of elastic arteries.

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Arterioles

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The smallest arteries that lead into capillary beds and are primary determinants of total peripheral resistance through changes in diameter. They play a central role in regulating local tissue perfusion and systemic blood pressure. Their smooth muscle responds to neural and chemical signals.

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Capillary Beds

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Networks of capillaries within tissues that permit exchange of gases, nutrients, and wastes between blood and cells. Precapillary sphincters control flow through individual capillaries. Capillary density matches tissue metabolic demand.

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Blood Pressure

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The force exerted by circulating blood on vessel walls, typically reported as systolic over diastolic pressure ($SBP/DBP$) in mmHg. It drives perfusion from high-pressure to low-pressure areas and is highest in the aorta. It is determined by cardiac output, total peripheral resistance, and blood volume.

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Cardiac Output

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The volume of blood pumped by each ventricle per minute, calculated as $CO = SV \times HR$ where $SV$ is stroke volume and $HR$ is heart rate. Higher $CO$ increases blood pressure if resistance remains constant. It reflects heart performance and metabolic demand.

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Total Peripheral Resistance

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The resistance to blood flow offered by the systemic vasculature, largely determined by arteriolar diameter and influencing blood pressure. Factors affecting it include blood viscosity, vessel length, and especially vessel diameter. Increased TPR raises blood pressure and reduces flow for a given cardiac output.

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TPR Factors

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Three major determinants of total peripheral resistance are blood viscosity, vessel length, and vessel diameter. Viscosity and length are relatively constant, but diameter changes via vasoconstriction or vasodilation dramatically alter resistance. Small changes in diameter produce large changes in TPR and BP.

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Baroreceptors

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Stretch-sensitive receptors located in arterial walls that detect changes in blood pressure and send afferent signals to the autonomic nervous system to adjust heart rate and vessel tone. Greater stretch increases their firing rate. They provide rapid feedback to maintain stable BP.

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Chemoreceptors

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Sensory receptors that detect changes in blood chemistry such as decreased $O_2$, increased $CO_2$, and decreased pH and influence respiration and cardiovascular responses. Peripheral chemoreceptors respond to blood gases; central chemoreceptors respond primarily to $CO_2$ and pH in cerebrospinal fluid. They supplement baroreceptor control under hypoxic or hypercapnic conditions.

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Autonomic Nervous System

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The involuntary nervous system that regulates cardiac rate, contractility, and vascular tone through sympathetic and parasympathetic divisions. Sympathetic activation increases $HR$, $CO$, and vasoconstriction via epinephrine/norepinephrine. Parasympathetic activation conserves energy and decreases heart rate.

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Renin-Angiotensin System

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A hormonal cascade activated by low blood pressure or volume: the kidneys release renin, which converts angiotensinogen to angiotensin I, then ACE converts it to angiotensin II. Angiotensin II causes vasoconstriction, stimulates aldosterone release to increase sodium and water retention, raises thirst, and increases ADH — all increasing BP.

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Aldosterone

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A mineralocorticoid hormone released from the adrenal cortex that increases sodium reabsorption and potassium excretion in the kidneys, leading to water retention and increased blood volume. This raises blood pressure. Some therapies aim to reduce aldosterone effects to lower BP and volume.

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Antidiuretic Hormone

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Also called ADH, a hypothalamic hormone released from the posterior pituitary that increases water reabsorption in the kidneys and can cause vasoconstriction. It helps conserve water and elevate blood pressure and volume in response to low BP or high osmolality. ADH contributes to short-term and longer-term BP control.

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Epinephrine/Norepinephrine

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Catecholamines secreted by the adrenal medulla that mediate the 'fight or flight' response by increasing heart rate, contractility, and vasoconstriction in many vascular beds. They increase stroke volume and cardiac output and thus raise blood pressure. Their effects are rapid and amplify sympathetic responses.

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Atrial Natriuretic Peptide

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A hormone released by atrial myocytes when atrial pressure or blood volume is high; ANP blocks renin and aldosterone and promotes sodium and water excretion. This results in decreased blood volume and blood pressure and causes vasodilation. It acts as a counter-regulatory system to RAAS.

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Renal Regulation

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Kidneys regulate blood pressure long-term by adjusting blood volume through urine production and salt/water balance. Increased salt or water intake raises blood volume and BP; dehydration or loss of volume reduces BP and triggers compensatory retention. Renal-mediated volume changes are central to chronic BP control.

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Blood Functions

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Transports oxygen and nutrients to cells, moves metabolic wastes to elimination sites, carries hormones to targets, regulates body temperature and pH, and maintains fluid balance. It also provides immune defense and hemostasis. Blood consists of plasma (about 55%) and formed elements (about 45%).

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Red Blood Cells

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Erythrocytes that transport oxygen from the lungs to tissues and help carry $CO_2$ back to the lungs, using hemoglobin as the oxygen-carrying protein. They have a lifespan of about 120 days and are produced continuously. RBCs greatly outnumber white blood cells.

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White Blood Cells

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Leukocytes that provide immune defense against infection and foreign materials and include granular (neutrophils, eosinophils, basophils) and agranular (monocytes, lymphocytes) types. Their lifespans range from hours to years depending on the cell type. They migrate to sites of infection or injury.

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Platelets

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Cell fragments involved in hemostasis with a lifespan of about 5–9 days that function in clotting, vascular spasms, and platelet plug formation. They adhere to damaged endothelium and aggregate to limit bleeding. Platelets also release factors that promote coagulation and vessel repair.

Front

Ejection Fraction

Back

The percentage of blood ejected from a ventricle with each heartbeat, calculated by $$EF=\frac{SV}{EDV}\times100\%$$ where $SV$ is stroke volume and $EDV$ is end-diastolic volume. It reflects ventricular systolic function and is measured by echocardiography. Normal ranges and thresholds help classify heart failure types.

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Stroke Volume

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The amount of blood ejected by a ventricle during a single contraction, equal to end-diastolic volume minus end-systolic volume ($SV = EDV - ESV$). It is influenced by preload, afterload, and contractility. Changes in stroke volume directly affect cardiac output.

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Myocardial Infarction

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Occurs when plaque in coronary arteries limits or stops blood flow to heart muscle, causing ischemic injury; plaques may rupture and trigger clot formation. MI can be STEMI (complete occlusion) or NSTEMI (partial occlusion). Prompt reperfusion and management are critical to limit damage.

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Stroke Types

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Three major types are ischemic (caused by blood clots blocking cerebral vessels), hemorrhagic (due to arterial rupture and bleeding into the brain), and transient ischemic attack (TIA), a brief temporary loss of blood flow producing transient neurologic symptoms. Etiologies and treatments differ by type.

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Hypertension

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Chronically elevated blood pressure measured in mmHg that forces the heart to work harder, causing left ventricular hypertrophy and increasing risk of myocardial infarction, heart failure, stroke, chronic kidney disease, and peripheral arterial disease. It damages artery walls and promotes atherosclerosis. Effective control reduces cardiovascular risk.

Front

Atherosclerosis

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A process of arterial wall thickening and loss of elasticity involving endothelial injury, cholesterol accumulation, macrophage foam cell formation, and smooth muscle/collagen deposition that forms plaque. Plaques can narrow the lumen or rupture to form occlusive clots. Risk factors include hypertension, hyperlipidemia, and smoking.

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Peripheral Artery Disease

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Atherosclerotic narrowing of arteries supplying the lower extremities that causes leg pain on exertion, impaired walking, and may lead to ischemic ulcers. It reflects systemic atherosclerosis and increases cardiovascular risk. Management includes risk factor control and revascularization when needed.

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Heart Failure

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A syndrome where the heart cannot pump sufficient oxygenated blood to meet body demands, leading to symptoms like dyspnea, fatigue, and fluid retention. It may involve systolic dysfunction (reduced contraction) or diastolic dysfunction (impaired relaxation) and is commonly caused by MI, CAD, and hypertension. Treatment includes lifestyle changes, medications, devices, and sometimes surgery.

Front

HFrEF

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Heart failure with reduced ejection fraction, defined as $EF<40\%$, characterized by impaired ventricular contraction and systolic dysfunction. It is more common in younger males and is often associated with prior MI and ischemic heart disease. Guideline-directed therapies (ARNI/ACE/ARB, beta-blockers, MRA, SGLT2, diuretics) improve outcomes.

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HFpEF

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Heart failure with preserved ejection fraction, defined as $EF\ge50\%$, often seen in older females with hypertension, obesity, and comorbidities; it involves diastolic dysfunction and stiff, thickened ventricular walls. Diagnosis is more challenging because EF is normal despite symptomatic heart failure. Management emphasizes diuretics, risk factor control, and selected therapies like SGLT2 inhibitors.

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HFmrEF

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Heart failure with mildly reduced ejection fraction where $LVEF$ is between 41% and 49%. It represents an intermediate group with features of both HFrEF and HFpEF and may benefit from therapies used in HFrEF depending on clinical context. Monitoring and individualized management are important.

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HFimpEF

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Heart failure with improved ejection fraction — a prior $LVEF<40\%$ that has subsequently increased above 40% on follow-up. This indicates partial recovery of systolic function but patients still require continued guideline-directed therapy and monitoring. Prognosis tends to be better than persistent HFrEF.

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Heart Failure Tests

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Diagnostic evaluation includes blood tests (e.g., natriuretic peptides), cardiac imaging (echocardiography to assess $EF$ and structure), ECG, pulmonary function and exercise tests, and sometimes advanced imaging. Echocardiography is essential to measure ejection fraction and chamber sizes. Testing guides classification and management.

Front

HF Management

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Treatment combines lifestyle modification, medications, device therapy, and surgical options. Core medication classes include RAAS inhibitors (ACE, ARB, ARNI), beta-blockers, mineralocorticoid receptor antagonists (MRA), SGLT2 inhibitors, and diuretics for volume control. Advanced cases may require revascularization, valve surgery, or transplantation.

Front

RAAS Inhibitors

Back

Drug classes that interrupt the renin-angiotensin-aldosterone system to reduce vasoconstriction, sodium retention, and remodeling; examples include ACE inhibitors (captopril, enalapril, lisinopril), ARBs (valsartan, losartan), and ARNIs (sacubitril/valsartan). They lower blood pressure and improve outcomes in HFrEF. MRAs like spironolactone and eplerenone block aldosterone effects.

Front

SGLT2 Inhibitors

Back

Antidiabetic drugs that inhibit sodium-glucose cotransporter-2 in the kidney, which also reduce preload and afterload, decrease sympathetic activity, and slow heart failure progression. They are recommended for many patients with heart failure regardless of diabetes status. They provide diuretic-like and cardioprotective benefits.

Front

Echocardiography

Back

A noninvasive imaging technique that assesses cardiac structure and function, including measurements of $EDV$, $ESV$, and $EF$. It's the primary diagnostic tool for evaluating heart failure type and severity. It also detects valvular disease and chamber enlargement.

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